Is it possible to demonstrate the impact of antireflux surgery on dysplastic changes of the mucosa?
T.C. Smyrk (Omaha)
Do sampling errors adversely effect our ability to monitor mucosal changes following antireflux surgery? The same question can be asked about follow-up of any therapy and the answer is more than a matter of academic curiosity. If regression or stabilization of dysplasia in Barrett's esophagus cannot be adequately documented, how can different modes of treatment be compared? Also, if progression cannot be documented, can the clinician and patient be comfortable choosing conservative treatment for a high-risk condition such as Barrett's esophagus with high-grade dysplasia?
Some sense of the difficulty in monitoring posttreatment changes in dysplasia can be gained by examining efforts to follow posttreatment changes in the length of Barrett's esophagus. Hassall and Weinstein recently reviewed previous reports claiming regression of Barrett's esophagus and found that all suffered from some deficiencies, such as poor identification of esophageal landmarks, inadequate pre- and posttreatment histology and inadequate documentation (i.e., pH studies) of therapeutic efficacy . When dysplasia is added to the equation, with its usual absence of gross changes and its dependence on subjective histologic interpretation, the problem becomes even more complex.
That complexity is reflected in prevailing attitudes about high-grade dysplasia in Barrett's esophagus. Due to fear that high-grade dysplasia might progress to advanced invasive carcinoma during follow-up or that high-grade dysplasia might be accompanied by undiagnosed adenocarcinoma at presentation, esophagectomy has been recommended in that setting . Recent work from the University of Washington suggests that observation can be a safe option . Levine et al. presented 22 patients followed with prospective endoscopic surveillance for Barrett's esophagus with high-grade dysplasia. There was no mortality from adenocarcinoma not diagnosed at an early stage (compared to an operative mortality of 14%). The authors argue that high-grade dysplasia alone does not necessarily require surgical resection.
The experience of the UW group can be applied to the question under consideration: Yes, it is possible to demonstrate the impact of antireflux surgery on dysplasia, provided the physician and the patient are willing to follow a rigorous biopsy protocol. Any attempt to monitor dysplastic Barrett's esophagus, following any type of treatment, must include the following:
1. Minimize the number of endoscopists involved in follow-up for better standardization.
2. Document the linear extent of Barrett's mucosa, based on accepted esophageal landmarks such as the Z line or the top of the LES.
3. Take multiple biopsies at each endoscopy in a systematic fashion.
The UW group recommends four quadrant biopsies taken every 1-2 cm over the entire length of Barrett's esophagus. In addition, multiple biopsies should be taken from sites at which high-grade dysplasia has been documented previously.
It can be hoped that improvements in adjunctive methods such as DNA analysis by flow cytometry will soon provide useful information in this setting. There may even come a day when areas of high-grade dysplasia can be labeled in vivo to allow endoscopic visualization. Until then, surveillance of high-grade dysplasia and assessment of posttreatment changes will depend on a carefully followed biopsy protocol and close co-operation between endoscopist and pathologist.